(livescience)–The protein that the coronavirus uses to attach to human cells has a compact “ridge” that allows it to attach more strongly to human cells than similar viruses, allowing it to infect better and spread faster, according to a new study.

The new coronavirus, SARS-CoV-2, attaches to human cells through what’s called a “spike protein,” according to a previous Live Science report. After the spike protein binds to the human cell receptor — a protein on the cell surface that serves as a door into the cell — the viral membrane fuses with the human cell membrane, allowing the genome of the virus to enter human cells.

All coronaviruses attach to human cells through spike proteins, but different coronaviruses have spike proteins with different structures. In February, a group of researchers at the University of Texas at Austin and at the National Institutes of Health mapped out the molecular structure of the new coronavirus’ spike protein, according to the report.

Now, another group of researchers used X-rays to further explore the coronavirus’ spike protein and the human cell receptor it binds to. Their goal was to understand why this coronavirus’ spike protein is so good at infecting cells, compared with a similar coronavirus, known as SARS-CoV, that caused the severe acute respiratory syndrome (SARS) outbreak in 2003.

This more compact structure, and several other small differences, allows SARS-CoV-2 to attach more strongly to the human ACE2 receptor, thereby enabling it to better infect cells and thus spread faster than the SARS coronavirus, according to the statement.

“In general, by learning what structural features of viral proteins are most important in establishing contact with human cells, we can design drugs that seek them out and block their activity — like jamming their radar,” Fang Li, a professor in the Department of Veterinary and Biomedical Sciences at the University of Minnesota, said in the statement.

By studying the specifics of this virus and how it attaches to cells, the researchers also gained some insights into how the virus may have hopped from animals to humans.

They discovered that a bat coronavirus also binds to the ACE2 receptor, but poorly. A few mutations could have increased the ability of the bat virus to attach to the human receptor, allowing the hop to humans, according to the statement. The researchers also analyzed the structure of the spike proteins of pangolins, which could be an intermediate host between bats and humans, according to a previous Live Science report.

They found that one of the pangolin coronaviruses could potentially bind to the human receptor, supporting the notion that pangolins were intermediate hosts of the virus. But that hypothesis would “need to be verified experimentally,” they wrote in the study.

As the novel coronavirus causing COVID-19 spreads across the globe, with cases surpassing 284,000 worldwide today (March 20), misinformation is spreading almost as fast.

One persistent myth is that this virus, called SARS-CoV-2, was made by scientists and escaped from a lab in Wuhan, China, where the outbreak began.

A new analysis of SARS-CoV-2 may finally put that latter idea to bed. A group of researchers compared the genome of this novel coronavirus with the seven other coronaviruses known to infect humans: SARS, MERS and SARS-CoV-2, which can cause severe disease; along with HKU1, NL63, OC43 and 229E, which typically cause just mild symptoms, the researchers wrote March 17 in the journal Nature Medicine.

“Our analyses clearly show that SARS-CoV-2 is not a laboratory construct or a purposefully manipulated virus,” they write in the journal article.

Kristian Andersen, an associate professor of immunology and microbiology at Scripps Research, and his colleagues looked at the genetic template for the spike proteins that protrude from the surface of the virus. The coronavirus uses these spikes to grab the outer walls of its host’s cells and then enter those cells. They specifically looked at the gene sequences responsible for two key features of these spike proteins: the grabber, called the receptor-binding domain, that hooks onto host cells; and the so-called cleavage site that allows the virus to open and enter those cells.

That analysis showed that the “hook” part of the spike had evolved to target a receptor on the outside of human cells called ACE2, which is involved in blood pressure regulation. It is so effective at attaching to human cells that the researchers said the spike proteins were the result of natural selection and not genetic engineering.

Here’s why: SARS-CoV-2 is very closely related to the virus that causes severe acute respiratory syndrome (SARS), which fanned across the globe nearly 20 years ago. Scientists have studied how SARS-CoV differs from SARS-CoV-2 — with several key letter changes in the genetic code. Yet in computer simulations, the mutations in SARS-CoV-2 don’t seem to work very well at helping the virus bind to human cells. If scientists had deliberately engineered this virus, they wouldn’t have chosen mutations that computer models suggest won’t work. But it turns out, nature is smarter than scientists, and the novel coronavirus found a way to mutate that was better — and completely different— from anything scientists could have created, the study found.

Another nail in the “escaped from evil lab” theory? The overall molecular structure of this virus is distinct from the known coronaviruses and instead most closely resembles viruses found in bats and pangolins that had been little studied and never known to cause humans any harm.

“If someone were seeking to engineer a new coronavirus as a pathogen, they would have constructed it from the backbone of a virus known to cause illness,” according to a statement from Scripps.

Where did the virus come from? The research group came up with two possible scenarios for the origin of SARS-CoV-2 in humans. One scenario follows the origin stories for a few other recent coronaviruses that have wreaked havoc in human populations. In that scenario, we contracted the virus directly from an animal — civets in the case of SARS and camels in the case of Middle East respiratory syndrome (MERS). In the case of SARS-CoV-2, the researchers suggest that animal was a bat, which transmitted the virus to another intermediate animal (possibly a pangolin, some scientists have said) that brought the virus to humans.

In that possible scenario, the genetic features that make the new coronavirus so effective at infecting human cells (its pathogenic powers) would have been in place before hopping to humans.

In the other scenario, those pathogenic features would have evolved only after the virus jumped from its animal host to humans. Some coronaviruses that originated in pangolins have a “hook structure” (that receptor binding domain) similar to that of SARS-CoV-2. In that way, a pangolin either directly or indirectly passed its virus onto a human host. Then, once inside a human host, the virus could have evolved to have its other stealth feature — the cleavage site that lets it easily break into human cells. Once it developed that capacity, the researchers said, the coronavirus would be even more capable of spreading between people.

All of this technical detail could help scientists forecast the future of this pandemic. If the virus did enter human cells in a pathogenic form, that raises the probability of future outbreaks. The virus could still be circulating in the animal population and might again jump to humans, ready to cause an outbreak. But the chances of such future outbreaks are lower if the virus must first enter the human population and then evolve the pathogenic properties, the researchers said.Coronavirus science and news

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